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G.B. is a 53-year-old white woman (height = 5 feet, 3 inches; weight = 170 pounds) with

hypertension, coronary artery disease, peripheral vascular disease, and diabetes, for which she
had been taking hydrochlorothiazide 25 mg PO daily, atorvastatin 10 mg POdaily, aspirin 81 mg
PO daily, and NPH insulin 30 units subcutaneously every morning and 15 units subcutaneously
every evening. At last week’s clinic visit, she had two consecutive BP readings of 187/96 and
193/95 mm Hg, respectively, measured 20 minutes apart. At that time, G.B.’s primarycare
physician discontinued her hydrochlorothiazide and started her on lisinopril 5 mg PO daily. She
returns to the clinic today for her 1-week follow-up appointment complaining of dizziness, verylittle urine production during the past week, and swelling in her ankles. Laboratory values and
vital signs obtained at this visit include the following:
BP, 98/43 mm Hg
BUN, 62 mg/dL
SCr, 6.1 mg/dL
2.1. Why is G.B. experiencing AKI?
2.2. Are there other factors that predispose patients to ACE inhibitor–induced AKI?
2.3. Do angiotensin II–receptor blockers (ARB) cause less AKI compared with ACE inhibitors?
2.4. How should G.B.’s ACE inhibitor–induced AKI be managed?

1 answer

2.1. Why is G.B. experiencing AKI?

G.B. is experiencing acute kidney injury (AKI) likely due to a combination of factors, primarily related to the initiation of the ACE inhibitor (lisinopril). ACE inhibitors can decrease renal perfusion pressure, especially in patients who have compromised renal function or severe hypertension. Given her history of coronary artery disease, diabetes, and the recent switch from hydrochlorothiazide (which can help control blood pressure and promote diuresis) to lisinopril, it is possible that her kidneys were not adequately perfused following the initiation of the ACE inhibitor.

The abrupt drop in blood pressure to 98/43 mm Hg is indicative of hypotension, which can further reduce renal blood flow and lead to AKI. Additionally, her symptoms of dizziness, minimal urine output, and ankle swelling suggest that she could be experiencing volume overload related to renal dysfunction.

2.2. Are there other factors that predispose patients to ACE inhibitor–induced AKI?

Yes, several factors can predispose patients to ACE inhibitor-induced AKI:

  1. Preexisting renal impairment: Individuals with chronic kidney disease (CKD) are at higher risk.
  2. Hypovolemia or dehydration: Decreased volume status can lead to a greater reduction in renal blood flow when starting an ACE inhibitor.
  3. Concurrent use of diuretics: Diuretics can lead to volume depletion, which exacerbates the risk of AKI when combined with ACE inhibitors.
  4. Malnutrition or low protein intake: This can contribute to a lower intravascular volume, heightening the risk for AKI.
  5. Heart failure: Patients with heart failure may have compromised renal perfusion.
  6. Age: Older individuals may have a reduced renal reserve.
  7. Diabetes: This condition can complicate kidney function and increase susceptibility to AKI.

2.3. Do angiotensin II-receptor blockers (ARBs) cause less AKI compared with ACE inhibitors?

In general, ARBs are thought to have a similar risk profile to ACE inhibitors when it comes to AKI. Both classes of medications can cause renal impairment, especially in patients with predisposing factors. However, some studies suggest that ARBs may have a somewhat better renal tolerance than ACE inhibitors, possibly because they do not affect bradykinin levels (which can cause side effects such as cough and angioedema). Nonetheless, ARBs can still cause AKI in susceptible individuals, similarly to ACE inhibitors.

2.4. How should G.B.’s ACE inhibitor–induced AKI be managed?

The management of ACE inhibitor-induced AKI involves several key steps:

  1. Discontinuation of the ACE inhibitor: Lisinopril should be stopped immediately to prevent further decline in renal function.
  2. Fluid resuscitation: If G.B. is volume-depleted (as suggested by low urine output and dizziness), intravenous fluids may be necessary to restore intravascular volume and improve renal perfusion.
  3. Monitoring renal function: Continuous monitoring of BUN and SCr is important to assess recovery and determine if further intervention is needed.
  4. Avoid nephrotoxins: G.B. should avoid any medications that may further compromise renal function, including nonsteroidal anti-inflammatory drugs (NSAIDs) and certain antibiotics.
  5. Adjust other medications: It may be necessary to adjust her diabetes medications (especially those cleared renally) and any antihypertensive therapy.
  6. Address underlying conditions: Managing her blood pressure and diabetes optimally will be crucial once renal function begins to recover.
  7. Consideration for alternative therapies: Once her renal function stabilizes, other blood pressure-lowering agents (once her volume status and renal function improve) can be considered, as appropriate.

Follow-up appointments will be essential to monitor her recovery and adapt her treatment plan based on her renal function and overall health status.